This document discusses explanations for questions from NBME 12 Block 1. It provides the question number, answer, and a multi-sentence explanation for each question from 1 to 17.
This document discusses explanations for questions from NBME 12 Block 1. It provides the question number, answer, and a multi-sentence explanation for each question from 1 to 17.
This document discusses explanations for questions from NBME 12 Block 1. It provides the question number, answer, and a multi-sentence explanation for each question from 1 to 17.
This document discusses explanations for questions from NBME 12 Block 1. It provides the question number, answer, and a multi-sentence explanation for each question from 1 to 17.
Hello everyone, some people use the offlines NBME as a tool for their tr aining while studying, since Maryam2009 discussion of this NBME is not longer available, i will begin t o post the answers and explanations of each question, following the one posted o n scribd. Any help is welcome as long as they contribute to the explanation and help clari fy doubts. Report Abuse
* Re:NBME 12 Block 1 q1-50 Discussion
#2951346 ae0704 - 09/15/13 16:01 Hello @sdfghjk, since there's a warning w/ copyright material in this fo rum, im not posting the questions stems, but as i hinted above, i am following t he order from the one posted in SCRIBD by user StepPrep. Please look for them there, and help yourself w/ some explanations here. Thank y ou. Report Abuse * Re:NBME 12 Block 1 q1-50 Discussion #2951362 ae0704 - 09/15/13 16:24 Q:10 Answer: D Spherocytosis: Intrinsic hemolytic normocytic anemia, caused by a defect in prot eins interacting with RBC membrane skeleton and plasma membrane (Ankyrin, band.3 .1 or spectrin). Autosommal Dominant. Pathogenesis: Less membrane=decrease membrane causes small and round RBC w/ no c entral pallor (Spherocytes) -->this is appreciated in the labs w/ the ? MCHC and RDW (indicates membrane loss and cell dehydration). This leads to premature removal of RBC by spleen (Characteristic accelerated RBC destruction). Presentation: Anemia, jaundice, splenomegaly (Due to RBC sequestration). Labs:Positive (+) Osmotic Fragility test, ? MCHC, RDW, Indirect bilirrubin and L DH. ? Haptoglobin Smear: Spherocytes and Howell-Jolly body after splenectomy. Assoc/ increase risk of Aplastic crisis (parvovirus b9 infx) and pigmented galls tones (bilirrubin gallstones) **prevent w/ splenectomy. Source: FA hemato. Report Abuse * Re:NBME 12 Block 1 q1-50 Discussion #2951366 ae0704 - 09/15/13 16:29
Q:11 Answer: B Vinblastine: MoA: Alkaloid that binds to tubulin in M phase and block Polymeriza tion= Assembly of microtubules so that mitotic spindle cannot form. Uses: Hodgkin L, Wilms tumor, Choriocarcinoma, ALL. Tox: Bone marrow suppression. Source: FA, Hemato. Report Abuse * Re:NBME 12 Block 1 q1-50 Discussion #2951378 ae0704 - 09/15/13 16:49 Q: 12 : "Insulin Slope in myocytes" Answer:B Insulin-responsive: GLUT-4, required for Adipose, skeletal muscle in order to up take glucose. The Y axis is the rate in which glucose is uptake by myocyte, Since the stem depict that the solid line correspond the absence of insulin, non e of the glucose is going to be uptake reason why we see the flat slope on the x axis, describing that there wasn't an uptake. and in the presence of insulin (dashed lines) the rate of uptake increases showi ng that when there's increases in insulin, GLUT-4 in those tissues, began to upt ake glucose inside in bigger rate.
Report Abuse * Re:NBME 12 Block 1 q1-50 Discussion #2951383 ae0704 - 09/15/13 16:59 Q: 13 Answer: A. Asperger Disorder: Milder form of Autism, Characterized by All-Absorbing interes ts, repetitive behavior and problems with social relationships. Childrens are of normal intelligence and lack verbal or cognitive deficits. No l anguage impairment. Source: FA pysch. Report Abuse * Re:NBME 12 Block 1 q1-50 Discussion #2951385 ae0704 - 09/15/13 17:05 Q:14 Answer: F Number Needed to treat (NNT)---->NNT=1/ARR (1)ARR=Exposed-Unexposed Assuming Trace elements as Control or Exposed:2.3% or 0.023 Unexposed: 1.3% or 0.013 ARR=0.023-0.013=0.01 (2)NNT=1/0.01= 100.
Report Abuse * Re:NBME 12 Block 1 q1-50 Discussion #2951392 ae0704 - 09/15/13 17:10 Q:15 Answer: E Herpes labialis: HSV-1: dss-DNA enveloped icosahedral. Causes gingivostomatitis, keratoconjuctivits, temporal lobe encephalitis, Herpes labialis. transmitted by respiratory secretions. Hides in the NEURONS of Trigeminal ganglia. Source: FA micro. Report Abuse * Re:NBME 12 Block 1 q1-50 Discussion #2951410 ae0704 - 09/15/13 17:29 Q:16 Answer: B in Anemia theres a Decrease in Hb, Hct or RBC concetration. SaO2 (oxygen saturation) and PaO2 are Normal. Decrease Oxygen Content (O2content). Please, clarify, not sure about the reason this is the answer, it was a lucky gu ess. Report Abuse * Re:NBME 12 Block 1 q1-50 Discussion #2951421 ae0704 - 09/15/13 17:41 Q:17 Answer: A Hepatitis B recombinant Vaccine: When the 2nd dose is given, sensitized cells fr om previous exposure (first dose) got stimulated and now secrete IgG. So there w ill be an increase of IgG:IgM ratio since immune system already recognize the an tigen. The IgG peak will occur earlier because of memory cells. An excellent example given by: @zen786 "an animal was injected with Antigen A at day 0. Antigen A invokes a primary res ponse beginning about day 4, as indicated by a rise in the specific antibody tit er (titer = measure of the amount of antibody in the animal's serum per unit vol ume). Initially, this antibody is mostly IgM (and some IgG). After a peak titer between days 7 and 10, the response decreases rapidly. If the animal is then rei njected with Antigen A at day 28, the production of antibody begins almost immed iately and reaches a level 1000-fold greater that that seen in the primary respo nse. This is known as the secondary response and the principal antibody produced is IgG. If a second antigen (Antigen B) is also injected at the same time as th e reinjection of Antigen A, however, only a primary response to Antigen B is obs erved. These results demonstrate that: The immune response is specific and that the immune response has memory.
immunoglobulin always primary at presentation of an antigen is IgM.... secondary
thats produced is always IgG unless mucuosal effected [IgA] or parastic infecti on [IgE]. IgG production will not be peaked in relation to IgM primarily. but after a second reinfection IgG will peak faster hence MEMORY*** of immunoglo bulin... IgM will be present but not likely in elevated state due to memory of b cell rel easing IgG right away... Later peak would not occur in a reinfection state.... LATER PEAK OF IgG can only be seen in a PRIMARY infection ... as you would see a later peak of IgG in "ant igen B" exposure in the example above...."
